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Cited by 1,053

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

IAP Antagonists Target cIAP1 to Induce TNFα-Dependent Apoptosis

Open access
Vince, James E., Wong, W. Wei-Lynn, Khan, Nufail, Feltham, Rebecca, Chau, Diep, Ahmed, Afsar U., Benetatos, Christopher A., Chunduru, Srinivas K., Condon, Stephen M., McKinlay, Mark, Brink, Robert, Leverkus, Martin, Tergaonkar, Vinay, Schneider, Pascal, Callus, Bernard A., Koentgen, Frank, Vaux, David L., Silke, John·2007·Cell
DOI 10.1016/j.cell.2007.10.037
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Abstract

XIAP prevents apoptosis by binding to and inhibiting caspases, and this inhibition can be relieved by IAP antagonists, such as Smac/DIABLO. IAP antagonist compounds (IACs) have therefore been designed to inhibit XIAP to kill tumor cells. Because XIAP inhibits postmitochondrial caspases, caspase 8 inhibitors should not block killing by IACs. Instead, we show that apoptosis caused by an IAC is blocked by the caspase 8 inhibitor crmA and that IAP antagonists activate NF-kappaB signaling via inhibtion of cIAP1. In sensitive tumor lines, IAP antagonist induced NF-kappaB-stimulated production of TNFalpha that killed cells in an autocrine fashion. Inhibition of NF-kappaB reduced TNFalpha production, and blocking NF-kappaB activation or TNFalpha allowed tumor cells to survive IAC-induced apoptosis. Cells treated with an IAC, or those in which cIAP1 was deleted, became sensitive to apoptosis induced by exogenous TNFalpha, suggesting novel uses of these compounds in treating cancer.

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Research works printed but not linked: 32

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Cited by

Metadata

Authors
Vince, J. E., Wong, W. W.-L., Khan, N., Feltham, R., Chau, D., Ahmed, A. U., Benetatos, C. A., Chunduru, S. K., Condon, S. M., McKinlay, M., Brink, R., Leverkus, M., Tergaonkar, V., Schneider, P., Callus, B. A., Koentgen, F., Vaux, D. L., & Silke, J.
Venue
Cell
Publisher
Elsevier BV
Published
2007-11
Volume
131
Issue
4
Pages
682-693
ISSN
0092-8674 (ISSN-L)
DOI
10.1016/j.cell.2007.10.037
OpenAlex
W2069800916
Cited by
1,053
References
3
FWCI
27.66
Type
journal article
Language
en
Open access
bronze
Licence

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